Allergy is a term commonly used to describe several forms of hypersensitivity. Hypersensitivity usually is classified into four types referred to by the Roman numerals I-IV. Types I to III hypersensitivities are mediated by antibodies and type IV is believed to be mediated by lymphocytes.
Asthma, hay fever, and eczema are considered to be of the type I form of hypersensitivity that is mediated by I.sub.g E antibodies and it is present in a significant percentage of humans. There is a general consensus that the mortality rates for asthma in much of the developed world have been increasing for the past 10-15 years. This increase has occurred despite an improved information base regarding diagnosis and management as well as the development of novel and more effective therapeutic modalities. Several explanations have been proposed for this increase, including a statistical artifact based on a change in the coding criteria for asthma from the International Classification of Diseases Version 8 to Version 9, worsened pollution, delays in seeking medical help, behavioral changes, deficits in asthma education of both patients and primary care providers, toxicity of beta agonists, and noncompliance with medications. It has been suggested that a change in our eating habits may contribute as well. The emphasis on reducing the intake of saturated fats and cholesterol has resulted in greater consumption of polyunsaturated fats and a consequent doubling of the percentage of the polyunsaturated linoleic acid in body fat. The only published results exploring the effects of dietary components on asthma show a positive effect of dietary fish oil on asthma and other inflammatory diseases.
The I.sub.g E mediated hypersensitivity or type I hypersensitivity also is sometimes referred to as "immediate hypersensitivity" because its effects are recognizable within minutes on rechallenge with antigen. It is dependent upon the binding of I.sub.g E antibodies to their receptors on mast cells and basophils. Cross-linking of the bound antibodies by antigen leads to the degranulation of the mast cells and basophils and to the synthesis of biologically active substances, which together with mediators, such as histamine, released from granules can cause an injurious form of inflammatory response.
It is not known with certainty what activates the mast cells and basophils to degranulate and to release the mediators from the granules. However, the degranulation or activation results in the release of prostaglandins and leukotrienes that are believed to be responsible for the clinical manifestations of the allergic reactions. Some of the mediators act upon other cells, such as eosinophils, neutrophils, monocytes, and lymphocytes to produce other substances which attack or are toxic to tissue and can lead to further clinical manifestations. Whatever the mechanism, the net result of a type I hypersensitivity attack can be very serious and even can be death.
It obviously would be advantageous to have both methods of attenuating the allergic response by preventing or inhibiting the adverse effects of type I hypersensitivity in an animal and methods for treating or alleviating such adverse effects.